Centrosomes, which consist of a centriole pair and pericentriolar[unreadable] material (PCM), are the key microtubule-organizing centers (MTOCs) in most cells. In Caenorhabditis elegans, the kinase ZYG-1 is essential for the replication of centrosomes. Embryos lacking maternal ZYG-1 activity fail to replicate the paternally contributed centriole pair, and are thus unable to form bipolar spindles following first division. In contrast, loss of paternal ZYG-1 activity results in duplication failure during male meiosis, and the production of sperm with a single centriole. These sperm can still fertilize eggs but the resulting embryos assemble a monopolar rather than bipolar spindle at first division. Several recently published reports indicated that centrosome duplication might be regulated differently in different tissues. To investigate this in C. elegans, we have been analyzing the effect of zyg-1 mutations on the male and female germ lines. We have found that small truncations of the c-terminus of ZYG-1 cause a novel phenotype: the production of embryos with supernumerary replication-incompetent centrosomes. These embryos inherit up to eight centrioles which are unable to duplicate. We have found the extra centrioles arise from defects in the male germ line and that this phenotype behaves as a gain of function. In contrast, failure of mutant embryos to duplicate these centrosomes is due to a loss of function of maternal ZYG-1. Thus, a single mutation behaves as a loss-of-function allele in one developmental context and a gain-of-function allele in another, suggesting that ZYG-1 is subject to different forms of regulation in different tissues. To gain insight into these regulatory mechanisms we are trying to determine the origin of these centrioles by studying centrosome duplication in the male germ line. So far we find that abnormalities in centrosome number are limited to the meiotic portion of the male germ line and have obtained evidence that centriole pairs are separating inappropriately. By comparing centriole behavior in the paternal and maternal germ lines of these zyg-1 mutants, we hope to determine how centrosome duplication might be regulated in a tissue-specific manner.